母体肠道细菌在小鼠后代中促进神经发育异常
Sangdoo Kim1, Hyunju Kim1, Yeong Shin Yim2
1Division of Infectious Diseases and Immunology and Program in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Nature
|September 14, 2017
概括
与神经发育障碍相关的母体免疫激活 (MIA) 需要促进T辅助17 (TH17) 细胞分化的肠道细菌. 这些细菌与母亲的免疫信号一起, 导致后代出现异常.
科学领域:
- 神经科学
- 免疫学
- 微生物学
背景情况:
- 孕产妇免疫激活与后代的神经发育障碍有关.
- 来自T助手17 (TH17) 细胞的IL-17a可以调解动物中MIA相关的异常.
- 其他母体因子和MIA诱导的T细胞激活机制的作用尚不清楚.
研究的目的:
- 研究母体肠道细菌在MIA相关的神经发育异常中的作用.
- 阐明MIA导致TH17细胞激活和IL-17a产生的机制.
主要方法:
- 用特定的肠道细菌 (细分细丝细菌或人类共生细菌) 殖民孕育的小鼠.
- 评估后代的行为和皮质异常.
- 分析母体小肠树突细胞的细胞因子分泌 (IL-1β,IL-23,IL-6).
主要成果:
- 母体感染TH17诱导细菌增加了MIA相关后代异常的发生率.
- 在后代中诱导IL-17a的产生.
- 暴露于MIA的怀孕小鼠显示小肠树突细胞增加IL-1β,IL-23和IL-6的分泌,刺激TH17细胞的分化.
结论:
- 诱导TH17细胞分化的母肠细菌对于后代的MIA相关神经发育表型至关重要.
- 确定的肠道开始性细菌可能会增加免疫激活的母亲后代的神经发育障碍的风险.
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